Present evidence indicates that prostaglandins (PG) mediate hyperreninemia, hyperaldosteronism and the vascular resistance to angiotensin II (AII) in Bartter's syndrome. The findings that prolonged treatment of a patient with Bartter's syndrome with an inhibitor of PG synthetase corrected the hyperreninemia and hyperaldosteronism but failed to correct the hypokalemia suggest that hypokalemia is not the result of aldosteronism per se and that hyperkalemia may be the cause of the hyperreninemia. This formulation is supported by the observation that patients with hypokalemia secondary to vomiting overproduced PGE2, have hyperreninemia, and are resistant to the pressor effects of AII. Studies of renal function in patients with hypokalemia indicate that those with Bartter's syndrome have an impaired distal tubular reabsorption of chloride, a finding best explained as a defect in chloride reabsorption in the loop of Henle, as judged by the clearances of solute free water and solute. This defect, which is PG-independent, could be the cause of potassium loss and, therefore, a proximal cause of the Syndrome. BIBLIOGRAPHIC REFERENCES: Bartter, F.C. Bartter's Syndrome. Urologic Clinics of North America 4: 253-261, 1977. Bartter, F.C., Gill, J.R., Jr. and Frolich, C. Le Syndrome de Bartter. Neckar Symposium: Flammarion Press, Paris, 1977.